摘要
以延边地区对磺酰脲类除草剂具抗、感性的慈姑为材料,采用RACE方法克隆了抗、感性慈姑的乙酰乳酸合酶(Acetolactate synthase,ALS)基因全长,分析了对除草剂抗、感性慈姑ALS基因c DNA编码区域的碱基差异,找出ALS基因的突变位点,为阐明慈姑对磺酰脲类除草剂抗性的突变机理提供分子依据。结果表明:与感性相比延边地区抗除草剂慈姑ALS基因共发生了7个碱基位点的突变,除了保守区域内第324位的苏氨酸(T3 24)突变为丙氨酸(A3 24)外,还包括非保守区域第17位的苏氨酸(T17)突变为脯氨酸(P17),而其他5个位点是氨基酸未改变的同义突变。这种错义突变和同义突变可能是延边地区抗性慈姑响应环境胁迫的分子基础。
To clarify the molecular mechanism of herbicide resistance in Yanbian, full length of Acetolactate synthase (ALS) genes eDNA to sulfonylurea of S. sagittifolia was cloned from resistant bio- type and susceptible biotype of S. sagittifolia with RACE method and the sequences were analyzed. The results showed that from seven mutational loci in the sulfonylurea-resistant biotype, threonine (T17) of the 17 th locus in the non-conservative area was replaced by alanine (P17), besides ,threo- nine (T324) of the 324 th locus was substituted by alanine (A324) in conservative domain, and the others were synonymous mutations. These missense and synonymous mutations may be the molecular basis for response of resistant S. sagittifolia to environmental stress in Yanbian.
出处
《吉林农业大学学报》
CAS
CSCD
北大核心
2015年第3期296-300,共5页
Journal of Jilin Agricultural University
基金
国家自然科学基金项目(31160370)
关键词
慈姑
乙酰乳酸合成酶
抗除草剂
分子机制
Sagittaria sagittifolia
acetolactate synthetase
herbicide resistance
molecular mecha-nism